Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BOBCAT Bronchial biopsy study

ABSTRACT: Clinical subphenotypes of asthma are characterized by pathological, cellular, and molecular heterogeneity of the airway. Gene expression profiling of affected tissues in diseased patients by microarray analysis will provide insight into the molecular heterogeneity and support the development of hypotheses of pathological mechanisms.

ORGANISM(S): Homo sapiens

PROVIDER: GSE79145 | GEO | 2017/08/23

SECONDARY ACCESSION(S): PRJNA315013

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Analysis of gene expression in human Bronchial Alveolar Lavage Cell (BAL) cell pellets

2016-01-06 | GSE74986 | GEO

Analysis of gene expression in human Bronchial Alveolar Lavage Cell (BAL) cell pellets

Project description:Clinical subphenotypes of asthma are characterized by pathological, cellular, and molecular heterogeneity of the airway. Gene expression profiling of airway inflammatory cells in diseased patients by microarray analysis will provide insight into the molecular heterogeneity and support the development of hypotheses of pathological mechanisms. Moderate asthmatic patients and healthy controls were participants in the Study of the Mechanisms of Asthma (MAST, clinicaltrials.gov: NCT00595153). Severe asthmatic patients were participants in the BOBCAT study (as described in Jia G JACI 2012 and Arron JR ERJ 2014). RNA (Qiagen AllPrep with on-column DNase treatment) was isolated from Bronchial Alveolar Lavage cells for gene expression microarray analysis.

2016-01-06 | E-GEOD-74986 | biostudies-arrayexpress

Small RNA profiling reveals deregulated PTEN/PI3K/Akt pathway in asthmatic bronchial smooth muscle cells

Project description:Background: Aberrant expression of small non-coding RNAs (sncRNAs), in particular microRNAs (miRNAs) and PIWI-interacting RNAs (piRNAs) define several pathological processes. Asthma is characterized by airway hyper-reactivity, chronic inflammation and airway wall remodeling. Asthma-specific miRNA profiles were reported for bronchial epithelial cells, but no information on sncRNA expression in asthmatic bronchial smooth muscle (BSM) cells is available. Objective: To determine whether primary BSM sncRNA expression profile is altered in asthma and identify targets of differentially expressed sncRNAs. Methods: SmallRNA sequencing was used for sncRNA profiling in BSM cells (8 asthma, 6 non-asthma). sncRNA identification and differential expression analysis was performed with iMir, . experimentally validated miRNA targets were identified with Ingenuity Pathway Analysis and putative piRNA targets with miRanda. Results: Asthmatic BSM cells showed abnormal expression of 32 sncRNAs (26 miRNAs, 5 piRNAs, and 1 snoRNA). Target prediction for deregulated miRNAs and piRNAs revealed experimentally validated and predicted mRNA targets expressed in the BSM cells. 38 of these mRNAs represent major targets for deregulated miRNAs and may play important roles in the pathophysiology of asthma. Interestingly, 6 such miRNAs were previously associated with asthma and/or considered as novel therapeutic targets for treatment of this disease. Signaling pathway analysis revealed involvement of these sncRNAs in increased cell proliferation via PTEN and PI3K/Akt signaling pathways. Conclusions: BSM cells from asthma patients are characterized by aberrant sncRNA expression that recapitulates multiple pathological phenotypes of these cells. Implications: sncRNA expression profiling performed in this study further improve our understanding of the molecular mechanisms underlying asthma-associated processes in lungs.

2018-01-07 | GSE64744 | GEO

Severe asthmatic bronchial smooth muscle decreases epithelial response to rhinovirus infection.

Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. We thus hypothesis that asthmatic BSM cells could act on bronchial epithelium and modified its response to rhinovirus infection.

2023-05-02 | PXD015604 | Pride

Asthma Bronchial Biopsy Gene Expression

Project description:Transcriptional profiling of lung bronchial biospsy mRNA from asthmatics Two-condition experiment, mRNA from asthma bronchial biopsies for test channel and Stratagene Universal Human Reference RNA for reference channel.

2015-09-08 | E-GEOD-69497 | biostudies-arrayexpress

The crucial role of CPT2 in the asthmatic bronchial smooth muscle remodeling

Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. Thus, we hypothesis that asthmatic BSM cell metabolism is modified compare to that of non-asthmatic and that could be a potential target to reduce asthmatic BSM cell proliferation and remodeling in asthma.

2021-06-10 | PXD015566 | Pride

Gu-Ben-Fang-Xiao decoction ameliorates airway remodeling by regulating the PI3K/AKT signaling pathway mediated by RTN4 in a chronic remission asthma murine model

Project description:Airway remodeling is a main pathological feature of asthma. The current therapy for asthma is mainly targeted for reducing inflammation, not particularly for airway remodeling. Herein, developing alternative and more effective therapy to attenuate remodeling is worthy of further study. Gu-Ben-Fang-Xiao Decoction (GBFXD) has been used to treat asthma for decades effectively and safely. In present study, GBFXD significantly regulated the airway inflammation, collagen deposition and the molecules relevant to airway remodeling such as Vimentin, α-SMA, hydroxyproline (HYP), and E-cadherin in chronic remission asthma (CRA) murine model. Subsequently, we found the overlapping differentially expressed proteins (DEPs) between Model/Control and GBFXD/Model mainly belonged to Collagen and Laminin which were extracellular matrix (ECM) proteins by iTRAQ proteomics. In addition, the KEGG analysis showed GBFXD could regulate pathways related to airway remodeling, such as ECM-receptor interaction, Focal adhesion, and PI3K/AKT signaling pathway which were top three pathways of most DEPs (Model/Control and GBFXD/Model) significantly enriched simultaneously. Further validation research showed GBFXD regulated Reticulon-4 (RTN4), thus suppressing the activation of PI3K/AKT pathway to alleviate the ECM proteins deposition. Thus, our findings indicate GBFXD regulate the PI3K/AKT pathway via RTN4 to improve airway remodeling and provide a new insight into the molecular mechanism of GBFXD for treating CRA.

2021-09-09 | PXD020711 | Pride

RNA-Seq expression analysis of chronic asthmatic mice with Bu-Shen-Yi-Qi formula treatment and prediction of regulated gene targets of anti-airway remodeling

Project description:Airway remodeling is one of the typical pathological characteristics of asthma. While, the structural changes of the airways in asthma are complex, which impedes the development of novel asthma targeted therapy. Our previous study have shown that Bu-Shen-Yi-Qi formula (BSYQF) could ameliorate airway remodeling in chronic asthmatic mice by modulating airway inflammation and oxidative stress in the lung. To further explore the molecular mechanism of BSYQF, in this study we analyzed the lung transcriptome of control, asthma mice with/without BSYQF treatment. Using RNA-sequencing analysis, we found that BSYQF treatment completely or partial reversed a group of genes that induced expression changes in asthma. Additionally, based on previous result we identified 21 differential expression genes (DEGs). Then through inputting 21 DEGs into Ingenuity Pathway Analysis (IPA) database to construct gene network, we inferred Adipoq, SPP1 and TNC which are located at critical nodes in the network, may be key regulators of BSYQF's anti-remodeling effect. Our results provide a preliminary clue to the molecular mechanism of anti-remodeling of BSYQF in asthma.

2021-01-01 | GSE155071 | GEO

Rhinovirus-induced modulation of gene expression in bronchial epithelial cells from subjects with asthma

Project description:Human Rhinovirus (HRV) infection can trigger exacerbations of asthma. Understanding of the mechanisms provoking airway inflammation and remodeling in asthma, as well as the pathogenic mechanisms of HRV infection and its association with asthma exacerbations, may offer significant opportunities for improved disease management. Genome-wide expression analysis of HRV type 1A-infected primary bronchial epithelial (PBE) cells from normal and asthmatic donors was performed to determine whether asthma is associated with a unique pattern of gene expression after HRV infection in vitro. Keywords: response to rhinovirus infection

2008-11-01 | GSE13396 | GEO

Changes in Expression of Genes Regulating Airway Inflammation Following a High-Fat Mixed Meal in Asthmatics

Project description:Consumption of a high fat meal can increase neutrophilic airway inflammation in asthma. This study investigates the molecular mechanisms driving airway neutrophilia following a high fat meal in asthma.

2015-10-16 | GSE74075 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data